Fructose & Sucrose-Obesity & Non-Alcoholic Fatty Liver
The following video is powerhouse of information by Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology on how particularly fructose ( fruit sugar) & sucrose (table sugar) is causing obesity and liver damage similar to alcohol, called Non-Alcholic Fatty Liver Disease.
It is long and somewhat complicated but is really worth the watch. The graphic below does a great job of summarizing the video.
It is long and somewhat complicated but is really worth the watch. The graphic below does a great job of summarizing the video.
Obese? A 'poisoned' food supply may be to blame,
UCSF expert says
Below is an excerpt of the San Fransico Gate article on the above video, definitely worth a read...
by Erin Allday, Chronicle Staff Writer
Saturday, August 12, 2006
The obesity epidemic may be caused by a "poisoned" food supply that is altering people's biochemistry and driving them to eat more and move less, according to a hypothesis proposed by a UCSF doctor who culled results from thousands of studies on obesity.
The processed food that is most readily available to Americans -- from potato chips and cookies to yogurt and white bread -- is loaded with sugars that cause the body to believe that it is hungry, which makes people feel compelled to consume more calories and conserve energy, he said. Sugar makes the body produce more insulin, which blocks hormones that would normally tell the brain to stop eating, he said.
About two-thirds of American adults are overweight, and about one-third are obese, according to the federal Centers for Disease Control and Prevention. Obesity is defined as being 20 percent to 25 percent over the ideal weight for one's height.
Doctors have long assumed that there is a connection between increasing sugar consumption and the country's out-of-control obesity epidemic. A study published in the American Journal of Clinical Nutrition earlier this week suggested that a single can of soda a day can add 15 pounds a year.
And increasingly, physicians are becoming frustrated with patients who are obese or in danger of becoming obese and seem incapable of making the lifestyle changes that are necessary to lose weight.
If Lustig's hypothesis is correct, then it's no wonder physicians are frustrated: Their patients are driven to eat more and exercise less, in much the same way they're driven to drink when they're thirsty.
"Your body is telling you to eat more. Our bodies don't do well fighting biochemical drive," Lustig said. "Try to not drink something after you've eaten a pizza, when you're thirsty."
The idea is that because consumers live in a "toxic environment" where sugar is a staple of so many food items, people are increasingly dependent on the sweetener, he said.
According to Lustig's hypothesis, sugar in large quantities drives up insulin secretion. This insulin floods the brain, and in particular the hypothalamus, which regulates energy use in the body. As a result, leptin, a hormone that tells the brain when the body needs more or less energy, can't get its signal to the hypothalamus because the insulin is blocking the way.
The result is that the body is thrown into starvation mode -- the brain thinks it isn't getting enough energy, so it needs more calories and it needs to save energy, he said. People end up feeling the symptoms of starvation, including malaise, depression, a lack of motivation and, of course, hunger.
"It's because of the toxic environment that the insulin rises and the problem behavior ensues," Lustig said. "That's why all of these diet programs don't work. That's why telling people to diet and exercise alone won't work, unless you improve the toxic environment as well."
Eating large amounts of sugar, says UCSF researcher Robert Lustig, tips the balance between insulin and the hormone leptin in the brain. Excess sugar makes the brain switch into starvation response mode. This prompts more eating and increases lethargy in order to conserve energy. The calories from more eating go unused and are stored as fat.
Starving for a drink...A hungry person drinks a soda (typically containing 10 teaspoons of sugar), and the body metabolizes that sugar. As a result, the pancreas increases insulin production. The brain, flooded with reports of increased insulin, decides to either turn the sugar into instant energy or store it as fat.
... AND NEVER FEELING FULL
After digesting the drink, the body should receive a signal of leptin from its fat cells. This signal tells the brain that the body has enough energy. However, large amounts of insulin may drown out the leptin signal, causing the hungry person to remain hungry.
by Erin Allday, Chronicle Staff Writer
Saturday, August 12, 2006
The obesity epidemic may be caused by a "poisoned" food supply that is altering people's biochemistry and driving them to eat more and move less, according to a hypothesis proposed by a UCSF doctor who culled results from thousands of studies on obesity.
The processed food that is most readily available to Americans -- from potato chips and cookies to yogurt and white bread -- is loaded with sugars that cause the body to believe that it is hungry, which makes people feel compelled to consume more calories and conserve energy, he said. Sugar makes the body produce more insulin, which blocks hormones that would normally tell the brain to stop eating, he said.
About two-thirds of American adults are overweight, and about one-third are obese, according to the federal Centers for Disease Control and Prevention. Obesity is defined as being 20 percent to 25 percent over the ideal weight for one's height.
Doctors have long assumed that there is a connection between increasing sugar consumption and the country's out-of-control obesity epidemic. A study published in the American Journal of Clinical Nutrition earlier this week suggested that a single can of soda a day can add 15 pounds a year.
And increasingly, physicians are becoming frustrated with patients who are obese or in danger of becoming obese and seem incapable of making the lifestyle changes that are necessary to lose weight.
If Lustig's hypothesis is correct, then it's no wonder physicians are frustrated: Their patients are driven to eat more and exercise less, in much the same way they're driven to drink when they're thirsty.
"Your body is telling you to eat more. Our bodies don't do well fighting biochemical drive," Lustig said. "Try to not drink something after you've eaten a pizza, when you're thirsty."
The idea is that because consumers live in a "toxic environment" where sugar is a staple of so many food items, people are increasingly dependent on the sweetener, he said.
According to Lustig's hypothesis, sugar in large quantities drives up insulin secretion. This insulin floods the brain, and in particular the hypothalamus, which regulates energy use in the body. As a result, leptin, a hormone that tells the brain when the body needs more or less energy, can't get its signal to the hypothalamus because the insulin is blocking the way.
The result is that the body is thrown into starvation mode -- the brain thinks it isn't getting enough energy, so it needs more calories and it needs to save energy, he said. People end up feeling the symptoms of starvation, including malaise, depression, a lack of motivation and, of course, hunger.
"It's because of the toxic environment that the insulin rises and the problem behavior ensues," Lustig said. "That's why all of these diet programs don't work. That's why telling people to diet and exercise alone won't work, unless you improve the toxic environment as well."
Eating large amounts of sugar, says UCSF researcher Robert Lustig, tips the balance between insulin and the hormone leptin in the brain. Excess sugar makes the brain switch into starvation response mode. This prompts more eating and increases lethargy in order to conserve energy. The calories from more eating go unused and are stored as fat.
Starving for a drink...A hungry person drinks a soda (typically containing 10 teaspoons of sugar), and the body metabolizes that sugar. As a result, the pancreas increases insulin production. The brain, flooded with reports of increased insulin, decides to either turn the sugar into instant energy or store it as fat.
... AND NEVER FEELING FULL
After digesting the drink, the body should receive a signal of leptin from its fat cells. This signal tells the brain that the body has enough energy. However, large amounts of insulin may drown out the leptin signal, causing the hungry person to remain hungry.
Robert H. Lustig, MD of Clinical Pediatrics, in the Division of Endocrinology Director of the Weight Assessment for Teen and Child Health (WATCH) Program at UCSF
Dr. Lustig is a nationally-recognized authority in the field of neuroendocrinology, with a specific emphasis on the regulation of energy balance by the central nervous system. He is currently investigating the contribution of biochemical, neural, hormonal, and genetic influences in the expression of the current obesity epidemic both in children and adults. He has defined a syndrome of vagally-mediated beta-cell hyperactivity which leads to insulin hypersecretion and obesity, and which is treatable by insulin suppression. This phenomenon may occur in up to 20% of the obese population. He is interested in the hypothalamic signal transduction of insulin and leptin, how these two systems interact, and how hyperinsulinemia contributes to leptin resistance. He is studying the cardiovascular morbidity associated with hyperinsulinemia, and developing methods to evaluate and prevent this phenomenon in children. He is also analyzing the contribution of the autonomic nervous system to insulin secretion and insulin resistance in obese children, and the utility of assessing insulin dynamics in targeting obesity therapy. Lastly, he is researching the role of specific macronutrients in fomenting liver insulin resistance and the metabolic syndrome, both in childhood and before birth.
Dr. Lustig graduated from MIT, and received his M.D. from Cornell University Medical College. He performed his pediatric residency at St. Louis Children's Hospital, and his clinical fellowship at UCSF. From there, he spent six years as a post-doctoral fellow in neuroendocrinology at The Rockefeller University in New York.
Dr. Lustig has authored over 85 research articles and 45 chapters. He is the former Chairman of the Obesity Task Force of the Pediatric Endocrine Society, a member of the Obesity Task force of The Endocrine Society, and on the Steering Committee of the International Endocrine Alliance to Combat Obesity. He is the Editor of the volume "Obesity before birth: maternal and prenatal effects on the offspring.
Dr. Lustig is a nationally-recognized authority in the field of neuroendocrinology, with a specific emphasis on the regulation of energy balance by the central nervous system. He is currently investigating the contribution of biochemical, neural, hormonal, and genetic influences in the expression of the current obesity epidemic both in children and adults. He has defined a syndrome of vagally-mediated beta-cell hyperactivity which leads to insulin hypersecretion and obesity, and which is treatable by insulin suppression. This phenomenon may occur in up to 20% of the obese population. He is interested in the hypothalamic signal transduction of insulin and leptin, how these two systems interact, and how hyperinsulinemia contributes to leptin resistance. He is studying the cardiovascular morbidity associated with hyperinsulinemia, and developing methods to evaluate and prevent this phenomenon in children. He is also analyzing the contribution of the autonomic nervous system to insulin secretion and insulin resistance in obese children, and the utility of assessing insulin dynamics in targeting obesity therapy. Lastly, he is researching the role of specific macronutrients in fomenting liver insulin resistance and the metabolic syndrome, both in childhood and before birth.
Dr. Lustig graduated from MIT, and received his M.D. from Cornell University Medical College. He performed his pediatric residency at St. Louis Children's Hospital, and his clinical fellowship at UCSF. From there, he spent six years as a post-doctoral fellow in neuroendocrinology at The Rockefeller University in New York.
Dr. Lustig has authored over 85 research articles and 45 chapters. He is the former Chairman of the Obesity Task Force of the Pediatric Endocrine Society, a member of the Obesity Task force of The Endocrine Society, and on the Steering Committee of the International Endocrine Alliance to Combat Obesity. He is the Editor of the volume "Obesity before birth: maternal and prenatal effects on the offspring.